Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructural changes induced by partial hepatectomy in the STH cells of mice were examined. These changes suggest an increased secretory activity of STH cells. Therefore, several experimental procedures elucidating the possible mechanism of this effect were undertaken. Normal mice were starved for 52 h or treated with insulin, glucagon, or cAMP. Serum glucose level measurements as well as electron microscopy of pituitary STH cells were carried out in each group of animals. It was found that STH cells of glucagon- and cAMP-treated mice showed some of the ultrastructural features observed in partially hepatectomized animals. Hence, serum hyperglucagonemia and increase in pituitary cAMP content, may be important components of the complex mechanism responsible for the ultrastructural changes in STH cells brought about by partial hepatectomy.
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PMID:Mechanism of the ultrastructural changes induced by partial hepatectomy in the STH cells of mice. 624 26

Insulin-induced hypoglycemias are a sign of non-sufficient counterregulation, in which different contra-insulinary hormones participate. The aim of the study was to investigate, whether there exists a difference between IDD and non-diabetics regarding secretion of glucagon, cortisol, and growth hormone during an insulin-induced hypoglycemia and further on pointing out, expecially, the importance of glucagon. Insulin-induced hypoglycemias are counterregulated in non-diabetics, not in IDD. The missing glucagon secretion during insulin-induced hypoglycemia in IDD seems to be independent from an autonomic neuropathy. Only after high doses of exogenous glucagon can one see a counterregulating increase of glucose. The STH secretion is similar in non-diabetics and IDD during an insulin-induced hypoglycemia and has evidently only a secondary effect in hypoglycemic counterregulation. The STH secretion may be the expression of a diencephal-triggered stress situation. The cortisol secretion is the same in both groups. The gluconeogenetic effect of cortisol is not sufficient to accomplish a fast compensation of hypoglycemia. This does not exclude long-term effects. When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias.
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PMID:[Glucagon, growth hormone, and cortisol response to insulin-induced hypoglycemia in insulin-dependent diabetics (IDD) without autonomic neuropathy (author's transl)]. 700 32

Fifty-five patients aged 15-35 years with insulin-dependent diabetes mellitus lasting 3.8 +/- 1.2 years underwent carbohydrate food loading. Within 2 hours after the meal, at 15-min intervals measurements were made of glycemia, C-peptide, insulin, glucagon, hydrocortisone, blood STH levels. Contrary to foodstuffs with low glycemia indices (GI), i.e. vermicelli, buckwheat, the intake of fast absorbed products with high GI (potatoes, hardtack, bread) stimulates glycemia and residual secretion of the islet cells. Enhanced entrance of gastrointestinal glucose into the systemic blood flow and growing insulinemia aroused glucagon secretion depression. The body responses to the above processes, assessed as metabolic stress, with increasing blood hydrocortisone and STH concentrations.
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PMID:[Products with high glycemic indices as factors in the metabolic stress of patients with insulin-dependent diabetes mellitus]. 790 57

The secretion of hormones stimulating and inhibiting gastric secretory activity was studied in 85 patients with postvagotomy syndromes. The somatropin level was found to increase significantly in gastrostasis. The lower values of the blood insulin and C-peptide content in patients with recurrent ulcers was evidently associated either with insufficiency of the pancreatic insular apparatus or with partial vagal denervation, increased STH level, and plausible inhibiting effect of glucagon. Increased somatostatin secretion in the dumping syndrome, gastrostasis, and peptic ulcers may be due to the encountered hypergastrinemia.
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PMID:[Neurohumoral regulation of gastric secretion in postvagotomy syndromes]. 793 83

Recently, hydrocortisone (HC) has been shown significantly to enhance interleukin-4 (IL-4)-induced in vitro IgE synthesis. For investigation of possible effects of synthetic corticosteroids but also of effects of other important human hormones, peripheral blood mononuclear cells (PBMC) were incubated with IL-4 and various concentrations of the hormones. IgE secreted in the supernatant was determined after a 14-d culture period. Like HC, all synthetic corticosteroids potentiated IgE secretion. A minor effect was noted for the mineralocorticoid aldosterone. No modulating effect on IL-4-induced IgE formation was observed for adrenocorticotropic hormone (ACTH), somatotropin (STH), thyroid-stimulating hormone (TSH), triiodothyronine, thyroxine, epinephrine, noradrenaline, insulin, and glucagon.
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PMID:Synthetic glucocorticoids potentiate IgE synthesis. Influence of steroid and nonsteroid hormones on human in vitro IgE secretion. 809 35

Repeated courses of hyperbaric oxygenation (HBO) were administered to 39 patients with insulin-dependent diabetes mellitus (IDDM) aged 28.2 +/- 11.3 years on an average and mean diabetes duration 5.7 +/- 0.5 years without body mass excess, administered insulin in daily dose 35.5 +/- 10.1. Control group consisted of 8 IDDM patients matched for clinical parameters and administered no treatment. Daily glucosuria, glycemia, HbA1, blood levels of e-peptide, glucagon, STH, and hydrocortisone were measured in the test group and controls before and after HBO course and every 2 months of a years's follow-up. Repeated courses of HBO administered to IDDM patients during a year are much more effective than a single course as regards diabetes compensation, reduction of insulin consumption, recovery of residual insulin secretion, and suppression of secretion of contrinsular hormones glucagon, STH, and hydrocortisone. Three courses of HBO therapy administered to IDDM patients at 4 months intervals are more effective than two courses with a 6 month interval; at the same time, in a three course modality the maximal positive effect of HBO on the hormonal metabolic status is attained during the second course, and the third course just fortifies the attained effect.
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PMID:[Efficacy of repeated courses of hyperbaric oxygenation in treatment of insulin-dependent diabetes mellitus]. 819 85

Seven days of dosing with either 30 mg or 60 mg of lansoprazole were compared with placebo in a double-blind, randomized, three-way cross-over study in 12 male healthy volunteers. Twenty-four-hour intragastric pH was measured after 7 days of dosing with each regimen, as well as 3 and 7 days after the end of dosing. During dosing with placebo, intragastric pH was above 4 for a median of 51 minutes. pH values were significantly raised to above 4 for 8.45 and 8.33 hours on Day 7 of dosing with lansoprazole 30 and 60 mg, respectively, but returned to normal by the third day after stopping dosing. No clinically relevant influence on endocrine function (serum concentrations of insulin, aldosterone, testosterone, parathormone, glucagon, T3, T4, TSH, LH, FSH, STH, prolactin, circadian cortisol profile, ACTH test) was observed. No serious adverse clinical or laboratory events were noted.
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PMID:The effects of lansoprazole, 30 or 60 mg daily, on intragastric pH and on endocrine function in healthy volunteers. 848 72

The glucagon like peptide-1 receptor (GLP-1R) agonist liraglutide attenuates induction of plasminogen activator inhibitor type-1 (PAI-1) and vascular adhesion molecule (VAM) expression in human vascular endothelial cells (hVECs) in vitro and may afford protection against endothelial cell dysfunction (ECD), an early abnormality in diabetic vascular disease. Our study aimed to establish the dependence of the in vitro effects of liraglutide on the GLP-1R and characterise its in vivo effects in a mouse model of ECD. In vitro studies utilised the human vascular endothelial cell line C11-STH and enzyme-linked immunosorbent assays (ELISA) for determination of PAI-1 and VAM expression. In vivo studies of vascular reactivity and immunohistochemical analysis were performed in the ApoE(-/-) mouse model. In vitro studies demonstrated GLP-1R-dependent liraglutide-mediated inhibition of stimulated PAI-1 and VAM expression. In vivo studies demonstrated significant improvement in endothelial function in liraglutide treated mice, a GLP-1R dependent effect. Liraglutide treatment also increased endothelial nitric oxide synthase (eNOS) and reduced intercellular adhesion molecule-1 (ICAM-1) expression in aortic endothelium, an effect again dependent on the GLP-1R. Together these studies identify in vivo protection, by the GLP-1R agonist liraglutide, against ECD and provide a potential molecular mechanism responsible for these effects.
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PMID:A GLP-1 receptor agonist liraglutide inhibits endothelial cell dysfunction and vascular adhesion molecule expression in an ApoE-/- mouse model. 2156 63


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